Stemmermann G, Heffelfinger S C, Noffsinger A, Hui Y Z, Miller M A, Fenoglio-Preiser C M
Department of Pathology and Laboratory Medicine, University of Cincinnati College of Medicine, OH 45267-0529.
Hum Pathol. 1994 Oct;25(10):968-81. doi: 10.1016/0046-8177(94)90056-6.
The evolution of sequential histological changes from normal cells through invasive cancer affords the cancer biologist the opportunity to identify separate molecular steps involved in cancer progression. As one studies the development of human carcinoma, it becomes apparent that multiple genetic alterations affecting both cellular proto-oncogenes and tumor suppressor genes are involved during the development and progression of both esophageal and gastric cancers. The different histological forms of both esophageal and gastric carcinomas as well as their differing etiologies result in the possibility that a spectrum of genetic changes is involved in different tumor types. p53 abnormalities occur frequently in tumors arising in both organs, and in both sites p53 abnormalities can be observed in precancerous lesions as well as in overt cancer. Subsequent abnormalities affecting other genes (eg, epithelial growth factor receptors [EGFRs]) potentially enhance the growth potential of tumors. This review focuses on abnormalities of oncogenes, tumor suppressor genes, and growth factors commonly found in cancers of the esophagus and stomach.
从正常细胞到浸润性癌的连续组织学变化的演变,为癌症生物学家提供了识别癌症进展中涉及的不同分子步骤的机会。当研究人类癌的发展时,很明显在食管癌和胃癌的发生和进展过程中涉及多种影响细胞原癌基因和肿瘤抑制基因的基因改变。食管癌和胃癌的不同组织学形式以及它们不同的病因,导致不同肿瘤类型可能涉及一系列基因变化。p53异常在这两个器官发生的肿瘤中经常出现,并且在这两个部位,癌前病变以及显性癌中都可观察到p53异常。随后影响其他基因(如上皮生长因子受体[EGFRs])的异常可能会增强肿瘤的生长潜力。本综述重点关注食管癌和胃癌中常见的癌基因、肿瘤抑制基因和生长因子的异常。